Als Beitrag zu der Frage der Korrelation zwischen peripherer arterieller Verschlußkrankheit (PAVK) und koronarer Herzkrankheit (KHK) ist die Häufigkeit von KHK in einer Gruppe von Patienten mit angiographisch dokumentierter PAVK und in einer Gruppe von Probanden ohne PAVK untersucht worden. Die Häufigkeit von KHK bei der PAVK-Gruppe beträgt 40.8% (86/211) gegenüber 18% (38/211) in der Kontrollgruppe (P < 0.005). Der Verlauf der KHK ist bei Patienten mit PAVK deutlich schwerer und häufiger letal als bei Probanden ohne PAVK. In der PAVK-Gruppe starben 30 Patienten an KHK gegenüber 2 Probanden der Kontrollgruppe.

Das Resultat zeigt, daß enge Beziehungen bestehen zwischen systolischer Hypertonie und Hyperlipidämie als Risikofaktoren und KHK. Die Häufigkeit von KHK in der Gruppe mit systolischer Hypertonie ist 38,4% (43/112) gegenüber 22,2% (69/310) in der Gruppe mit normalem Blutdruck. Es besteht auch ein signifikanter Unterschied in der Häufigkeit von KHK zwischen Probanden mit und ohne Hyperlipidämie, 45,8% (22/48) gegenüber 28,1% (105/374).

Andererseits konnte zwischen Rauchern und Nicht-Rauchern sowie zwischen Diabetikern und Nicht-Diabetikern kein signifikanter Unterschied in der Inzidenz von KHK gefunden werden.

Two to five μ1 20–50% horseradish peroxidase (HRP) in normal saline solution have been injected into the myocardium of the left ventricle of 36 rats. HRP positive reaction granules in spinal ganglion cells have been observed by means of DAB method.

Im Zeitraum von 20 Jahren (1955 bis 1975) wurden 1480 Fälle von Zervixkarzinom bestrahlt. Es überlebten 987 von 1480 (66,7%) 5 Jahre. Im Stadium I wurde eine 5-Jahres-Überlebensrate von 86,3%, im Stadium II eine solche von 73,4% und im Stadium II von 56% erreicht. Die Prognose bei Patientinnen mit Adenokarzinom und in Assoziation mit Gravidität wird analysiert. Es ist selbstverständlich, daß frühe Erkennung der Erkrankung und eine weitgehende Individualisierung der Behandlung für jede Patientin wichtige Maßnahmen zur Verhütung des Therapieversagens sind.

Concentrations of K⁺, Na⁺ and Mg⁺⁺ were measured in plasma (K⁺_e, Na⁺_e, Mg⁺⁺_e) and in erythrocytes (K⁺_i, Na⁺_i, Mg⁺⁺_i) in patients with digitalis toxicity before and after administration of Mg. K⁺ concentration in 24-hour urine was also measured. 70 persons were divided into 5 groups: (1) 11 normal persons as controls; (2) 19 patients with congestive heart failure, in whom Mg⁺⁺_i and Mg⁺⁺_e concentrations were found to be lower than that of the control group; (3) 16 patients with digitalis toxicity treated by Mg⁺⁺, whose K⁺_i concentration increased much quicker, and Na⁺_i and Na⁺_i/K⁺_i decreased remarkably in comparison to non-Mg treatment group; (4) 12 patients with digitalis toxicity not treated by Mg⁺⁺: in these the above-mentioned changes were not significant; (5) 12 patients with arrhythmia of other causes treated by Mg⁺⁺: whose K⁺_i also increased significantly on the 3rd day after treatment.

K⁺ concentration in 24-hour urine was much lower in Mg treatment group than in non-Mg treatment group.

Besides, acute digitalis toxicity was observed in experimental dogs. The concentration of K⁺_i recovered much quicker in Mg treatment group than in control group.

These findings indicate that hypomagnesemia may induce digitalis toxicity. In this paper the possible mechanism of the therapeutic effect of Mg in the treatment of digitalis toxicity is discussed.

Levels of thyroid hormones (T₃,T₄) in serum and cyclic adenosine 3′, 5′-monophosphate (cAMP) and cyclic guanosine 3′, 5′-monophosphate (cGMP) in plasma were successively determined in 77 patients with hyperthyroidism before and 1, 2, 3, 6 months after¹³¹iodine (¹³¹I) treatment. Before treatment, the levels of total serum T₃, T₄ and plasma cAMP of all of the patients were higher than normal, while the level of plasma cGMP was lower than normal (P<0.0l). The patients were divided into 3 groups: A, B, C, according to the clinical features and serum levels of T₃, T₄ 3–6 months after treatment. Group A (18 patients) clinically showed no improvement, T₃, T₄ still remained higher than normal and cAMP, cGMP revealed no significant change in comparison with the pretreatment state. Group B (45 patients) clinically showed marked improvement, their thyroid toxic symptoms practically subsided, T₃, T₄ gradually turned to normal and concentration of cAMP and cGMP subsequently reached normal level. Group C (14 patients) presented temporary hypothyroidic features; their level of T₃, T₄ fell below the normal range, while the concentration of plasma cAMP and cGMP approached the level contrary to the state before treatment. Since the change of T₃ and T₄ occurred synchronously, the question of whether T₃ or T₄ exerted an influence on plasma cyclic nucleotides concentration and the interrelationship between thyroid hormones and cyclic nucleotides as well as the significance of plasma cAMP and cGMP in pathogenesis and therapy of hyperthyroidism remains to be further elucidated.

This study was designed to investigate the levels of testis tissue cyclic nucleotides and plasma testosterone in testis-irradiated rats with saturation analysis 1–52 days after 676 rad and 7 days after 290–1930 rad. It was found that ionizing radiation of a given dose scale did not affect significantly the excretion of testosterone. An initial rise of cyclic adenosine monophosphate (cAMP) was probably associated with an increase of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) excretion and a decrease of cAMP in the later stage was possibly due to the depletion of the germ cells, following irradiation less than 965 rad. The reduction of cAMP after 1930 rad was probably related to direct inhibition of the larger dose of cAMP production. These results suggest that the levels of cAMP after irradiation can reflect the degree of testis radiation injury. In addition, it was also found that ionizing radiation failed to change the testis cyclic guanosine monophosphate (cGMP) levels, suggesting the presence in testis of only a “one-way” regulation carried out by cAMP.